3D printed guide-assisted percutaneous screw fixation for minimally displaced scaphoid waist fractures with delayed diagnosis or presentation.

OBJECTIVES: To Investigate the value of 3D printed guide-assisted percutaneous management of minimally displaced scaphoid waist fractures(Herbert's B2) with delayed diagnosis or presentation. METHODS: From October 2018 to February 2022, 10 patients with established delayed diagnoses and presentation of minimally displaced scaphoid waist fractures were treated with 3D printed guides assisted with percutaneous internal fixation without bone grafting. This technique was based on the patient's preoperative CT and imported into the software. Based on Boolean subtraction, the most centralized screw placement position was identified and a customized guide was produced. Intraoperative percutaneous insertion of the guide wire was assisted by the custom guide. RESULTS: All 10 patients were successful in one attempt. The fractures healed at a mean of 7.7 weeks postoperatively (range 6-10 weeks). At a mean follow-up of 7.7 months (6-13 months), patients had excellent recovery of wrist function with minimal pain reduction. There were no major postoperative complications and the patients all returned to their previous activities before the injury. CONCLUSIONS: Percutaneous internal fixation based on 3D printed guides is a safe and effective technique for delayed diagnosis or presentation of patients with minimally displaced fractures of the scaphoid waist. This method allows for easy insertion of screws and avoids multiple attempts.

HAGLR, stabilized by m6A modification, triggers PTEN-Akt signaling cascade-mediated RPE cell pyroptosis via sponging miR-106b-5p.

Consistent hyperglycaemia on retinal microvascular tissues is recognized as a vital inducer of diabetic retinopathy (DR) pathogenesis. In view of the essential functionality of long noncoding RNAs (lncRNAs) in multiple human diseases, we aim to figure out the exact role and underlying mechanisms of lncRNA HOXD Cluster Antisense RNA 1 (HAGLR) in DR pathogenesis. Serum specimens from patients with proliferative DR and healthy volunteers were collected for measuring HAGLR levels. Human primary retinal pigment epithelium (HRPE) cells kept in high glucose (HG) condition were applied to simulating hyperglycaemia of DR pathology in vitro. Cell proliferation, apoptosis, either pyroptosis was assess using Cell Counting Kit-8 TUNEL, flow cytometry, and enzyme-linked immunoassay assays. Bioinformatics analysis was subjected to examine the interaction between HAGLR and N6-methyladenosine (m6A)-bind protein IGF2BP2, as determined using RNA immunoprecipitation and RNA pull-down. Luciferase reporter assay was performed to assess the HAGLR-miR-106b-5p-PTEN axis. Levels of pyroptosis-associated biomarkers were detected using western blotting. Aberrantly overexpressed HAGLR was uncovered in the serum samples of DR patients and HG-induced HRPE cells, of which knockdown attenuated HG-induced cytotoxic impacts on cell apoptosis and pyroptosis. Whereas, reinforced HAGLR further aggravated these effects. IGF2BP2 positively regulated HAGLR in a m6A-dependent manner. HAGLR served as a sponge for miR-106b-5p to upregulate PTEN, thereby activating Akt signaling cascade. Rescue assays demonstrated that PTEN overexpression abolished the inhibition of silenced HAGLR on pyroptosis in HRPE cells. HAGLR, epigenetically modified by IGF2BP2 in an m6A-dependent manner, functioned as a sponge for miR-106b-5p, thereby activating PTEN/Akt signaling cascade to accelerate DR pathology.

Bilateral carpal tunnel syndrome and motor dysfunction caused by gout and type 2 diabetes: A case report.

BACKGROUND: Carpal tunnel syndrome (CTS) has been associated with gout and type 2 diabetes mellitus (T2DM). However, due to insufficient clinical understanding of gout-related CTS and reliance on the diagnostic importance of elevated serum uric acid levels, such cases are prone to missed diagnosis, misdiagnosis, and delayed treatment. In addition, the effect of T2DM on gout - induced carpal tunnel syndrome has not been reported. CASE SUMMARY: Herein, we present an unusual case of CTS and motor dysfunction caused by miliary tophaceous gout and T2DM. The patient presented to the hand and foot clinic with paresthesia of the fingers of both hands, especially at night. The patient was diagnosed with type 2 diabetes a month ago. Ultrasonography revealed bilateral transverse carpal ligament thickening with median nerve compression during hospitalization. The patient was successfully treated with carpal tunnel decompression and tendon release. The postoperative pathological examination revealed typical gout nodules. This case suggests that the presence of T2DM could accelerate tophi formation and worsen CTS symptoms, although no definitive proof in this regard has been described previously. CONCLUSION: Tophi formation may most likely cause the co-occurrence of CTS and flexor dysfunction in gout and incipient diabetes patients.

Minimally Invasive Percutaneous Screw Guided by 3-Dimensional-Printed Guide for the Treatment of Scaphoid Fractures.

PURPOSE: This study aimed to explore the feasibility and efficacy of percutaneous fixation of minimally displaced scaphoid waist fractures using a 3-dimensional-printed guide in 10 cases. METHODS: Fractures were examined using preoperative computed tomography. The skin interface and bone models were reconstructed using computed tomography data. Guidewire insertion was assisted by a guide. Computed tomography was performed 4-6 weeks after surgery until healing of the fracture was confirmed. The mean follow-up period was 7 months (range, 6-9 months). The fracture healing time, grip strength, flexion-extension arc, patient-rated wrist evaluation, and Mayo wrist score were recorded. RESULTS: A total of 6 hands were in the dominant limb. The mean operation time was 41 minutes (range, 32-70 minutes). Three (30%) scaphoids healed at 6 weeks after surgery, 8 (80%) scaphoids healed at 8 weeks after surgery, and 100% scaphoids healed at 12 weeks after surgery. After correcting for hand dominance, the mean grip strength was 84% (range, 71% to 95%) of that of the contralateral side. The flexion-extension arc was 97% (range, 82% to 100%) of that of the contralateral side. The mean Mayo wrist score was 95 (range, 85-100), and pain decreased to minimal levels. All patients returned to their preinjury activities. CONCLUSIONS: Three-dimensional printing is an effective and feasible technology that can help guide intraoperative processes. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic V.

Miconazole alleviates peripheral nerve crush injury by mediating a macrophage phenotype change through the NF-κB pathway.

BACKGROUND: Peripheral nerve injury (PNI) causes motor and sensory defects, has strong impact on life quality and still has no effective therapy. Miconazole is one of the most widely used antifungal drugs; the aims of the study were to investigate the effects of miconazole during sciatic nerve regeneration in a mouse model of sciatic nerve crush injury. METHODS: We established peripheral nerve crush model and investigated the effects of miconazole by multiple aspects. We further studied the potential mechanism of action of miconazole by Western blotting, fluorescence immunohistochemistry, and PCR analysis. RESULTS: Miconazole improves the symptoms of crushed nerve by improving inflammatory cell infiltration and demyelinating myelin of sciatic nerve. Affected by miconazole, the proportion of inflammatory M1 macrophages in the distal part of the sciatic nerve was reduced, and the proportion of anti-inflammatory M2 macrophages was increased. Finally, the neuroprotective properties of miconazole may be regulated by the nuclear factor (NF)-κB pathway. CONCLUSIONS: Our data suggest that miconazole can effectively alleviate PNI, and the mechanism involves mediating a phenotype change of M1/ M2 macrophages. Thus, miconazole may represent a potential therapeutic intervention for nerve crush injury.

Functional sequence variants within the SIRT1 gene promoter in indirect inguinal hernia.

Inguinal hernia is a common surgical disease, for which genetic factors have been suggested to play a role. Sirtuin 1 (SIRT1), a highly conserved NAD-dependent class III deacetylase, has been implicated in human diseases. Since SIRT1 regulates differentiation and proliferation of human skeletal muscles and fibroblasts, we speculated that misregulation of SIRT1 gene, caused by DNA sequence variants (DSVs) within its regulatory regions, may contribute to inguinal hernia development. In this study, SIRT1 gene promoter was genetically and functionally analyzed in patients with indirect inguinal hernia (IIH) (n=139) and ethnic-matched healthy controls (n=148). Two heterozygous DSVs, g.69644213G>A and g.69644268T>A, and one single nucleotide polymorphism (SNP), g.69643707A>C (rs35706870), were found in IIH patients, but not in controls. Two closely-linked SNPs, g.69644217A>C (rs932658) and g.69644341G>C (rs2394443), were found in IIH patients with significantly higher frequency, compared to controls (P=0.006). The C alleles of the SNPs g.69644217A>C (rs932658) and g.69644341G>C (rs2394443) were associated with IIH (P=0.028, OR 1.600, 95%CI 1.049-2.439). These DSVs significantly altered the transcriptional activities of the SIRT1 gene promoter in cultured cells. Therefore, our data suggested that these DSVs may alter the transcriptional activities of SIRT1 gene promoter and change SIRT1 levels, contributing to IIH development as risk factors.

Genetic analysis of the TBX1 gene promoter in indirect inguinal hernia.

Inguinal hernia is a common disease, most cases of which are indirect inguinal hernia (IIH). Genetic factors play an important role for inguinal hernia. Increased incidences of inguinal hernia have been reported in patients with 22q11.2 microdeletion syndrome, which is mainly caused by TBX1 gene mutations. Thus, we hypothesized that altered TBX1 gene expression may contribute to IIH development. In this study, the human TBX1 gene promoter was genetically analyzed in children with IIH (n=100) and ethnic-matched controls (n=167). Functions of DNA sequence variants (DSVs) within the TBX1 gene promoter were examined in cultured human fibroblast cells. The results showed that two heterozygous DSVs were found, both of which were single nucleotide polymorphisms. One DSV, g.4248 C>T (rs41298629), was identified in a 2-year-old boy with right-sided IIH, but not in all controls, which significantly decreased TBX1 gene promoter activity. Another DSV, g.4199 C>T (rs41260844), was found in both IIH patients and controls with similar frequencies (P>0.05), which did not affect TBX1 gene promoter activity. Collectively, our data suggested that the DSV within the TBX1 gene promoter may change TBX1 level, contributing to IIH development as a rare risk factor. Underlying molecular mechanisms need to be established.